ReviewInternational journal of molecular sciences2025
Molecular and Cellular Mediators of Renal Fibrosis in Lupus Nephritis.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Article
- Damaged glomeruli in proliferative pediatric lupus nephritis exhibit a C5a-C5aR1 induced fibrotic transcriptional program.bioRxiv : the preprint server for biology · 2026Article
- Evaluating Chronicity Scores for Outcomes in Patients With Lupus Nephritis.Kidney international reports · 2026Article
- Circulating long non-coding RNAs as diagnostic markers of lupus nephritis and 5-year follow-up disease flares.Frontiers in immunology · 2026Article
- HE4: a potential diagnostic biomarker in autoimmune diseases.Central-European journal of immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Lupus nephritis (LN), a significant complication of systemic lupus erythematosus (SLE), represents a challenging manifestation of the disease. One of the prominent pathophysiologic mechanisms targeting the renal parenchyma is fibrosis, a terminal process resulting in irreversible tissue damage that eventually leads to a decline in renal function and/or end-stage kidney disease (ESKD). Both glomerulosclerosis and interstitial fibrosis emerge as reliable prognostic indicators of renal outcomes. This article reviews the hallmarks of renal fibrosis in lupus nephritis, including the known and putative drivers of fibrogenesis. A better understanding of the cellular and molecular processes driving fibrosis in LN may help inform the development of therapeutic strategies for this disease, as well as the identification of individuals at higher risk of developing ESKD.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.